This Article Full Text Full Text (PDF) CME: Take the course for this article: Circulation: May 13, 2008, Volume 117, Number 19 All Versions of this Article: 117/19/2475    most recent CIRCULATIONAHA.107.719500v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shah, S. J. Articles by Gomberg-Maitland, M. Search for Related Content PubMed PubMed Citation Articles by Shah, S. J. Articles by Gomberg-Maitland, M. Related Collections Cardio-renal physiology/pathophysiology Pulmonary circulation and disease Epidemiology Related Article

(Circulation. 2008;117:2475-2483.)
© 2008 American Heart Association, Inc.

Epidemiology

Association of Serum Creatinine With Abnormal Hemodynamics and Mortality in Pulmonary Arterial Hypertension

Sanjiv J. Shah, MD; Thenappan Thenappan, MD; Stuart Rich, MD; Lu Tian, ScD; Stephen L. Archer, MD; Mardi Gomberg-Maitland, MD, MSc

From the Division of Cardiology, Department of Medicine (S.J.S.) and Department of Preventive Medicine (L.T.), Northwestern University Feinberg School of Medicine, Chicago, Ill; and Section of Cardiology, Department of Medicine (T.T., S.R., S.L.A., M.G.-M.), University of Chicago, Chicago, Ill.

Correspondence to Mardi Gomberg-Maitland, MD, MSc, Director of Pulmonary Hypertension, University of Chicago, 5841 S Maryland Ave, MC 2016, Chicago, IL 60637. E-mail mgomberg{at}medicine.bsd.uchicago.edu

Received June 5, 2007; accepted March 12, 2008.

Background— Renal dysfunction predicts mortality in patients with cardiovascular disease. How renal dysfunction relates to hemodynamics and mortality in pulmonary arterial hypertension (PAH) remains unclear.

Methods and Results— We performed a cohort study of 500 patients with World Health Organization group I PAH from 1982 to 2006 with data on demographics, comorbidities, medications, functional class, laboratory tests, exercise testing results, and hemodynamics. Serum creatinine (SCr) was determined on entry into the study (initial PAH clinic visit). Vital status was determined from hospital records and the Social Security Death Index. We used a Cox proportional hazards analysis to determine whether SCr was an independent predictor of mortality. Mean age on entry into the study was 48±14 years, and 79% of subjects were female. Mean SCr was 1.05±0.35 mg/dL. Elevated SCr was associated with higher right atrial pressure and lower cardiac index. During a median follow-up of 3.5 years, 279 deaths (55.8% of the cohort) occurred. Compared with patients with SCr <1.0 mg/dL, those with SCr 1.0 to 1.4 mg/dL and SCr >1.4 mg/dL had an increased hazard ratio of death (unadjusted hazard ratio 1.65, 95% confidence interval 1.26 to 2.17, P<0.0001 for SCr 1.0 to 1.4 mg/dL; unadjusted hazard ratio 2.54, 95% confidence interval 1.73 to 3.71, P<0.0001 for SCr >1.4 mg/dL). On multivariable analysis, we found a significant interaction between SCr and right atrial pressures (interaction P<0.0001); increased SCr best predicted death in patients with right atrial pressure <10 mm Hg.

Conclusions— Renal dysfunction is associated with a worse hemodynamic profile and is an independent predictor of mortality in PAH. Measurement of SCr is practical and offers a simple way to noninvasively predict outcome.

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CLINICAL PERSPECTIVE

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